The goal of this project is to understand spinal cord mechanisms that regulate arterial pressure, with special attention to the roles of the sympathetic nervous system after spinal cord injury and recovery or after spinal cord regeneration. In patients after spinal injury, ordinarily innocuous stimuli, such as a full colon, may cause autonomic dysreflexia, hypertensive crises, stroke, and death. An additional cardiovascular threat is presented by the prospect of spinal cord regeneration. If this regeneration is not appropriate and specific, attempts to move may result in large increases in arterial pressure. These two dangers, one very immediate and the other potentially occurring in the near future require a far better understanding of the processing of sympathetic activity in the spinal cord. For the first time, we have adapted the method of cross correlation to the identification of spinal interneurons that are candidates for belonging to spinal sympathetic networks. We have used this method to study the relationship between the ongoing activity of spinal interneurons and sympathetic nerve activity in anesthetized rats and discovered that, after spinal transection the activities of a large proportion of interneurons are synchronous with sympathetic activity, indicating that large networks in the spinal cord may be responsible for generating sympathetic activity after spinal transection. During the renewal of this project, we will direct our effort at three Aims. In Aim 1, we will use the new method of juxtacellular labeling to describe the exact positions and detailed morphology of sympathetically correlated neurons. In Aim 2, we will determine the relationships between neurons that generate sympathetic activity before spinal transection and those that generate activity after spinal transection. In Aim 3, we will trace the pathways from the pelvic organs, especially the colon and bladder that ascend to the levels of sympathetic preganglionic neurons and elicit hypertensive crises after spinal transection.